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. Author manuscript; available in PMC: 2018 Dec 12.
Published in final edited form as: Nat Rev Immunol. 2013 Oct 11;13(11):777–789. doi: 10.1038/nri3536

Figure 3 |. T-bet expression in ILCs and DCs in the intestines.

Figure 3 |

Innate lymphoid cells (ILCs) and T-bet-expressing dendritic cells (DCs) interact in the colonic lamina propria to maintain epithelial integrity. T-bet (encoded by Tbx21) represses tumour necrosis factor (TNF) expression in colonic DCs. In the absence of T-bet, TNF from DCs causes colonic epithelial cell apoptosis in the context of the pathobiont, Helicobacter typhlonius. TNF from DCs cooperates with interleukin-23 (IL-23) to induce interferon-γ (IFNγ) and IL-17 expression from ILCs. T-bet expression in ILCs regulates the plasticity of cytokine responses by repressing IL-17 and by inducing IFNγ production. This pathology creates an inflammatory milieu that generates a dysbiotic microbiota that is capable of transmitting colonic inflammation to wild-type mice. Dashed line indicates that the developmental relationship between these ILC subsets is unclear. CCR6, CC-chemokine receptor 6; NKp46, NK cell p46-related protein; RORγt, retinoic acid receptor-related orphan receptor-γt.